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. 2019 Apr 4;8(8):e010823. doi: 10.1161/JAHA.118.010823

Figure 1.

Figure 1

Loss of Cx37−/− alters the increase in blood pressure in models of renin‐dependent hypertension. A, WT mice receiving daily 1 mg Ang II/kg body weight displayed a 50% increase in systolic blood pressure (SBP). Under the same conditions, Cx37−/− mice displayed a significantly lower increase of SBP. WT NaCl N=5; Cx37−/− NaCl, WT Ang II (angiotensin II), Cx37−/− Ang II N=6. B, Similar observations were made in mice receiving daily 0.25 mg Ang II/kg body weight WT NaCl, Cx37−/− NaCl N=7; WT Ang II, Cx37−/− Ang II N=8. C, Two weeks after the 2K1C (2‐kidney, 1‐clip) procedure, Cx37−/− mice also showed a lower increase in SBP than WT controls. WT sham (sham‐operated controls) WT 2K1C, N=5; Cx37−/− sham, Cx37−/− 2K1C N=6. D, In contrast, both types of mice became similarly hypertensive after a treatment with l‐NAME (N‐nitro‐l‐arginine‐methyl‐ester); N=6. ***P≤0.001 vs corresponding controls (NaCl‐infused or sham‐operated animals); °°° P≤0.001 vs WT mice, as given by 2‐way ANOVA of AUC (areas under the SBP curve). Ang II indicates angiotensin II; Cx37, connexin37; WT, wild type.